The relationship between specific immune responses and tumor growth and rejection will be investigated. The P815-X2 tumor is lethal in DBA/2 mice from whom the tumor was derived. F1 hybrids of that strain, namely B6D2F1, do respond to the P815-X2 tumor and after a substantial period of subcutaneous growth, the tumor is rejected. It would appear that this response is directed against a tumor-specific antigen and that the response is genetically controlled. The number of genetic loci involved in controlling this response will be determined with backcross mice. The genetic sites or the lymphoid cell subpopulation(s) expressing this control will be ascertained from transfer studies involving various combinations of specifically fractionated cells from "nonresponder" and responder mice. The lymphoid cell subpopulation responsible for the "immunostimulation" effect or augmented tumor growth will be studied, especially the possibility that they may function as "suppressor" cells. The presence of the "immunostimulatory" cells in nonresponder mice will be examined. It may be that these cells are those most affected by the genetic 'defect' that limits the level of response in the "nonresponder" mice.